Fact Sheet: Poisonous Plants For Cattle

Many poisonous plants emerge in the early spring before grasses begin to grow. During cool wet springs, poisonous plants often gain an advantage over the grasses and if livestock are turned out too early, poisoning may occur. This is especially true for low larkspur, lupines, water hemlock and poison hemlock. Low larkspur is short-lived and high risk in early spring, and once seeds have shattered very little risk from low larkspur remains. Tall larkspurs are often high risk in early to mid summer when the flower/seed heads are prevalent. Storm episodes often drive cattle into areas where tall larkspur is prevalent and large cattle losses may result. Nightshades, while they emerge early, are more likely a contaminant of harvested forages than a risk for pasture-grazing animals. The toxin does not degrade in hay or silage.

These fact sheets provide information about symptoms of each plant toxicity, when and where the plants usually occur, how they affect livestock and how you can reduce loss.

The greatest risk of lupine is “crooked calf syndrome,” caused by pregnant cows or heifers grazing certain lupines during late first trimester or early second trimester. The species of lupine and the alkaloid profile is required to evaluate risk. Cows may give birth to calves with cleft palate and skeletal defects if the cows ingest certain lupines during early gestation (crooked calf syndrome), during the 40 th to the 100 th day of gestation.

Poisonous species of lupine are toxic from the time they start growth in spring until they dry up in fall. Younger plants are more toxic than older plants; however, plants in the seed stage in late summer are especially toxic because of the high alkaloid content of the seeds. Lupines are legumes and are relatively high in protein, especially the seed pods, and may become a preferred forage species when grasses become mature and dry. Under proper conditions, some lupines make good forage.

Where and when lupines grow:

Lupines grow on foothills and mountain ranges in sagebrush and aspen areas. Lupine populations expand during wet seasons and may die back during dry seasons. The seed reserve in the soil remains high and when environmental conditions are optimum lupine population will increase.

How lupines affect livestock:

The amount of lupine that will kill an animal varies with species and stage of plant growth. It is not safe to let sheep freely graze certain species and the early flower/seed pod stage of plant growth is especially dangerous.

Overt poisoning in cattle occasionally occurs if cattle lack other feed. Signs of poisoning and resultant death depends on the alkaloid content of the plant, how rapid the lupine is ingested and for how long. Smaller amounts may be poisonous if cattle eat lupine daily for 3 to 7 days. The major issue for cattle is the birth defects (crooked legs, spine or neck and/or cleft palate). Pregnant cows/heifers must graze some lupine over multiple days during the sensitive stages of pregnancy (40-100 days for cleft palate and skeletal deformities, or 40-50 days for cleft palate only) for deformities to occur.

How to reduce losses:

Poisoning can be reduced by keeping hungry animals away from lupines in the early growth stage, in late summer when the plant is in the highly toxic seed stage, and from dense plant stands at all times. Supplemental feeding is beneficial, especially when animals are trailed through lupine ranges. If animals are poisoned on lupines, do not try to move them until they show signs of recovery.

If cows in the susceptible gestational period (40th to 100th days of gestation) are kept from lupine when it is most teratogenic (very early growth or mature seed stage), most deformities can be prevented. The congenital deformity hazard is minimal at other gestation periods and after seeds have shattered from pods. The malformations can be avoided by adjusting the breeding season and the grazing of lupine-infested range to avoid the critical periods of gestation.

There is no known treatment for lupine poisoning, except removing the animal from the source and keep the animal calm until recovery occurs..

Lupine can be controlled with 2,4-D (2 lbs. ae/acre), 2,4-D + dicamba (1 + 0.5 lbs. ae/acre), or triclopyr (0.5 to 1.5 lbs. ae/acre). Spray actively growing plants after they are 5 in. high but before they bloom. Reinvasion is rapid and retreatment may be necessary every 4 to 5 years.

Fact Sheet: Death Camas

Signs and lesions of death camas poisoning:

Salivation and bloody frothing

Nausea and vomiting

Muscular weakness and staggering

Pulse fast and weak

Prostration, labored breathing, gasping

Coma

Death due to heart failure

Death within a few hours to a few days

Congestion of lungs and kidneys

Minimal necrosis of skeletal and cardiac muscle

Death camas (Zigadenus spp.) is the common name of several species of plants that are poisonous to livestock. The more toxic of these species are grassy death camas (Z. gramineus), meadow death camas (Z. venenosus), foothill death camas (Z. paniculatus), and Nuttall's death camas (Z. nuttallii). They are found principally in the western range states.

Death camas is one of the first plants to begin growth in early spring. Without sufficient other forage, death camas may be heavily grazed and will cause severe losses. Spring snow storms may cover all forage except death camas, which may protrude through the snow and is available to the livestock. Sheep are most likely to be affected by feeding on death camas. Occasionally, cattle and horses are poisoned.

Death camas contains toxic steroidal alkaloids that occur throughout the plant; plants are dangerous at all times.

The bulb may be mistaken for those of the edible camas or quamash (Cammassia spp.) and can cause severe illness in humans. If bulbs are eaten, take the affected person to the emergency room of the nearest hospital immediately.

Where and when death camas grows:

Some species of death camas thrive on sandy soils; others grow on drier, rocky foothills. The more toxic species are seldom found above elevations of 8,000 ft. Death camas grows early in spring, matures, and enters dormancy during early summer when soil moisture declines.

The leaves appear very early in the spring. In the foothills, death camas generally flowers in April and May. At higher elevations, the plant may flower in late June and July.

How death camas affect livestock:

Death camas causes marked disturbance in respiration and heart action. A 100-lb. sheep may die if it eats ½ to 2 lb of green foliage. The amount of foliage that will cause an animal’s death depends on the species of plant eaten and the rate of consumption. Severely poisoned animals usually die; those less seriously affected may recover.

How to reduce loss:

To avoid poisoning, delay turnout until adequate good forage is available. Do not introduce hungry sheep into heavy stands of death camas. Avoid feeding, bedding, or trailing sheep through heavy stands of death camas.

There is no known treatment for death camas poisoning.

Research results show that early in the season, when plants have three to six leaves, death camas can be controlled by spraying with 2,4-D at the rate of 1½ to 3 lbs. ae/acre. After the flowering stalks appear, spraying is not effective.

There are several species of nightshades that are toxic to horses, cattle, swine, sheep and poultry. The genus includes annual and perennial herbs and shrubs that can be found throughout the U.S.

The principal species that serve as examples of the genus are black nightshade (Solanum nigrum), silverleaf nightshade (S. eleagnifolium), and buffalo burr (S. rostratum). Black nightshade is an introduced herbaceous annual weed that can be found growing mostly on disturbed soils and waste areas in the eastern U.S. and into the Midwest. Silverleaf nightshade is a perennial with long creeping rootstocks. Buffalo burr is an annual native to the Great Plains and introduced to the West Coast.

The toxins include a combination of a number of sugars and at least six different steroidal amines combined to form a variety of glycoalkaloids. One example is the toxin solanine. Potatoes are included with this group because the vines are toxic and tubers that have been exposed to light can be toxic to livestock. Drying does not destroy the toxin.

Nightshade species are not very palatable to livestock. However, these plants often grow as weeds in hay and silage crops and small grains where they can be harvested with the crop and then fed to livestock.

Where and when nightshades grow:

Black nightshade (both the native and introduced varieties) is an annual 6 in. to 3 ft. tall. Leaves are simple, ovate to lanceolate, entire to sinuate-dentate. Flowers are white; berries are black when ripe. It grows peripherally in moist areas of fields and pastures of disturbed loamy or gravelly soils throughout the U.S.

Silverleaf nightshade is a perennial that grows 1 to 3 feet tall with white, hairy leaves and stems. Leaves are simple, thick, lanceolate to linear, entire to sinuate. Stems and ribs usually have short stiff spines. Flowers are violet or blue; berries are yellow or orange. Silverleaf nightshade grows in fields, pastures, and roadsides from Missouri to Texas and California.

Buffalo burr is an annual spiny weed 1-2 ft. tall. Leaves are irregularly round-lobed or once or twice pinnately deeply lobed; veins are spiny. Flowers are yellow, and the berries are enclosed. Native to the Great Plains and introduced to the West Coast, buffalo burr grows in old fields, overgrazed pastures and roadsides.

How nightshades affect livestock:

Nightshades are generally unpalatable and are not grazed by livestock except under the stress of overgrazing or in contaminated hay and grain. Poisoning by this group of plants does not always end in death. In acute poisoning, the nervous symptoms develop rapidly. Death or recovery occurs within a few hours to 1 or 2 days. Death apparently is related to the paralysis. Chronic poisoning is accompanied by emaciation, rough hair coat, anorexia, constipation and ascites.

How to reduce loss:

Losses can be kept at a minimum by good pasture management and weed control. Harvested forage such as hay, grain or silage can be contaminated with nightshades. Contaminated forage can be fed if it is diluted (mixed) with nightshade-free forage: an on/off feeding strategy should be used. Animals being fed this diluted forage should be kept under close surveillance and immediately removed from the contaminated feed if signs of poisoning appear. Submit a sample to the Poisonous Plant Research Lab for analysis.

Fact Sheet: Poison Hemlock

Signs and lesions of poison hemlock poisoning:

Nervous trembling

Neuromuscular stimulation followed by depression and paralysis

Ataxia, especially lower and hind limbs

Salivation

Lack of coordination

Dilation of the pupils

Rapid, weak pulse

Respiratory paralysis

Coma

Death

Convulsions have been reported

Occasionally bloody feces and gastrointestinal irritation

Skeletal birth defects and cleft palate in calves and piglets if cows or sows eat poison hemlock during susceptible stage of gestation: 40th to 100th days for cows, 30th to 60th days for sows

Poison hemlock (Conium maculatum) can be found growing throughout the U.S. Sheep, cattle, swine, horses and other domestic animals are poisoned by eating a small amount. It is also extremely poisonous to humans.

Poison hemlock is sometimes confused with western waterhemlock--a more deadly plant--because the names are similar. (See waterhemlock chapter in this volume.) Poison hemlock has a number of common names, including deadly hemlock, poison parsley, spotted hemlock, European hemlock, and California or Nebraska fern.

Roots of poison hemlock may be mistaken for wild parsnips and eaten by people. The stem of poison hemlock has purple spots on it.

All parts of poison hemlock--leaves, stem, fruit and root--are poisonous. Leaves are especially poisonous in spring up to the time the plant flowers. Fresh leaves are unpalatable, so livestock seldom eat hemlock when other feed is available. The tox­ic compounds are coniine, γ‑coniceine and related piperidine alkaloids.

Where and when poison hemlock grows:

Because of its attractive flowers, poison hemlock was brought to the U.S. from Europe as a garden plant but has escaped cultivation and can be found growing in many pastures and in some areas on rangeland. Poison hemlock is found at roadsides, along fences and ditch banks, on edges of cultivated fields, along creekbeds and irrigation ditches, and in waste areas. It may invade fields or pastures.

Poison hemlock is a biennial and belongs to the carrot family. It starts growing in early spring but does not flower until its second year. In favorable locations it may be a perennial. Poison hemlock harvested with hay can be toxic to livestock and produce birth defects.

How poison hemlock affects livestock:

Poison hemlock ingestion is often fatal. Sheep may be poisoned by eating as little as 4-8 oz. of green leaves. Cattle that eat 10-16 oz. may be affected. Signs usually appear within an hour after an animal eats the plant. Animals die from respiratory paralysis in 2 to 3 hours. Convulsions, which are common in waterhemlock poisoning, seldom occur with poison hemlock.

Skeletal deformities or cleft palate may be induced in offspring of cows, sheep, goats and pigs if poison hemlock is ingested by the mother during susceptible stage of gestation: 40th to 100th days in cows and 30th to 60th days in sheep, goats and pigs. Palate and skeletal deformities in calves are indistinguishable from the lupine-induced crooked calf disease.

How to reduce loss:

Avoid stressing poisoned animals that are not recumbent. For recumbent animals, support respiration and treat with activated charcoal and a saline cathartic. Gastric lavage may be beneficial, with atropine therapy to control parasympathetic signs.

Animals that recover seldom show lingering effects.

Research results show that poison hemlock may be controlled by treating plants before they begin to bud with 2,4-D plus dicamba (2.5 lbs. + 1 lb. ae/acre). Repeat applications may be needed.

Fact Sheet: Waterhemlock

Signs and lesions of water hemlock poisoning:

Nervousness

Excessive salivation and frothing

Muscle twitching

Dilation of the pupils

Rapid pulse

Rapid breathing

Tremors

Violent convulsions, grand mal seizures

Coma

Death may occur as early as 15 minutes after a lethal dose is consumed

No significant gross lesions

Water hemlock (Cicuta douglasii) is the most violently toxic plant that grows in North America. Only a small amount of the toxic substance in the plant is needed to produce poisoning in livestock or in humans. The toxin, cicutoxin, acts on the central nervous system and is a violent convulsant.

Water hemlock may be confused with poison hemlock because of their similar flowers. However, these two are different plants and cause different types of poisoning. (See poison hemlock chapter in this fact sheet.)

The underground portions of the plant, especially the tuberous roots, are very toxic. People are sometimes poisoned by eating the roots, which they mistake for wild parsnip.

In cases of water hemlock poisoning in humans, take the affected person to the emergency room of the nearest hospital immediately. Call poison control and seek emergency treatment immediately.

Cattle have been known to eat lethal amounts of water hemlock in pastures having adequate forage; therefore, animals should be prevented from grazing over water hemlock-infested areas. Animals have been poisoned by eating roots that have been brought to the surface by plowing or cleaning ditches.

The toxic substance in water hemlock is cicutoxin, a highly poisonous unsaturated alcohol that has a strong carrot-like odor. It is found principally in the tubers but is also present in the leaves, stems, and immature seeds. Leaves and stems lose most of their toxicity as they mature.

Where and when water hemlock grows:

Water hemlock is most commonly found growing in wet meadows and pastures and along stream banks. It starts growing in spring. Water hemlock usually flowers in June or July.

How water hemlock affects livestock:

Livestock usually show signs of poisoning 15 minutes to 6 hours after eating the plant. They develop violent convulsions and may die within 15 minutes to 2 hours after signs appear.

How to reduce loss:

The toxic substances act so rapidly that an affected animal can seldom be saved. Treatment consists of preventing seizures with barbiturates or tranquilizers and supporting respiration. Gastric lavage, activated charcoal, or saline cathartic may be helpful. Seek immediate medical or veterinary treatment.

To reduce losses, keep animals away from places where water hemlock grows. Prevent water hemlock poisoning in livestock by carefully surveying pastures and ranges at a time when the plant can be identified, and eradicate it.

The plants, which usually grow in small patches, are easy to locate. They can be eradicated by spraying or grubbing. Actively growing plants can be controlled with 2,4-D at 2 lbs. ae/acre. Repeat spray treatments until eradication is complete. The stems and leaves of water hemlock increase in palatability immediately after being sprayed with herbicide. Therefore, keep animals away from treated plants for 3 weeks after spraying. Most losses occur early in the spring or after the plants have been sprayed with 2,4-D.

Note: If grubbing the water hemlock, use gloves and be careful to get all of the plant, including roots. Gather and burn every part, don’t leave tubers lying around.[14]

Fact Sheet: Larkspurs (tall and low)

Tall larkspurs tend to grow at higher elevations on deep soils where a plentiful supply of moisture is available. They grow in mountain meadows on sites where deep snowdrifts persist well into the growing season, under aspens on north-facing slopes, along streams, or around seeps and springs. Tall larkspur begins growing as soon as snow melts, but at the upper limits of their distribution this may not occur until July.

Low larkspurs tend to grow at lower elevations where they mature and become dormant before the soil moisture is depleted. They begin growing in early spring, often before other forage begins growth. Low larkspurs grow best when springs are cold and wet. Cattle will graze low larkspur at all stages of growth, but most often graze it after flowering.

Plains larkspur is found primarily on the high plains of Colorado and Wyoming. It begins growth in spring before other plants.

How larkspur affects animals:

Plains larkspur may be eaten by cattle at any time during summer, but early green growth and pods may be most appealing to cattle. Both low and plains larkspurs may be the only green herbage available to cattle in early spring.

The larkspurs contain a number of alkaloids of varying toxicity. The most toxic of these are the MSAL (methyl succidimino acetyl lycoctonine) types, which include methyllycaconitine. Submit a sample to the Poisonous Plant Research lab for analysis.

How to reduce loss:

Placing an af­fected animal on its brisket or chest with its head uphill may reduce bloating. Treatment for bloat (intubation or rumen puncture with a trocar) may save some animals. Avoid unduly exciting affected animals.

Toxicity of tall larkspurs declines as it matures through the growing season. Research has identified a toxic window of high risk during the flower and early pod stages when it becomes palatable and toxin levels are moderate.

Since cattle do not generally consume tall larkspurs before flowering, grazing early before plants flower may be an acceptable grazing option. Cattle should be moved off of the larkspur areas during the flower stage but can graze larkspur in the late pod stage when toxicity declines. Using sheep to graze or trample tall larkspur patches ahead of cattle grazing may reduce cattle losses.

Low larkspur losses may be prevented by deferring grazing until plants lose their flowers and pods, as they rapidly senesce after producing pods. This usually occurs in late spring or early summer and grazing is safe after seed shatter.

The cholinergic drug neostigmine (0.02 mg/kg i.m.) has been successfully used under pen conditions to reverse clinical larkspur intoxication. This reversal lasts about 2 hours, and repeated injections of neostigmine are sometimes required. Under field conditions, neostigmine temporarily abates clinical signs and animals quickly (about 15 minutes) become ambulatory. Depending on the larkspur dose, the intoxication can resurface. Nonetheless, there are risks associated with the use of neostigmine. The use of neostigmine-based treatments may actually aggravate losses in the absence of further treatment because suddenly mobile animals may later develop increased muscular fatigue and dyspnea and may die.

Research results show that low lark­spurs can usually be controlled by applying 2,4-D at the rate of 4 lbs. ae/acre when the vegetative development approaches its maximum but before the first flowers open.

Tall larkspur can be controlled with picloram (1 to 2 lbs. ae/acre) up through the flowering stage. Metsulfuron (1-2 oz. of product/acre) is effective when applied in the early vegetative stage of growth. Plains larkspur can be controlled with picloram (0.25 to 0.5 lb. ae/acre) in the bud stage.

Do not graze cattle on larkspur ranges treated with herbicide until larkspur is senescent in the fall. Herbicide treatment may increase palatability to cattle, but toxicity remains high.